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Chances are you know someone with obsessive-compulsive disorder (OCD). It’s estimated that more than 2 million Americans struggle with this mental health condition, characterized by unwanted recurring thoughts and/or repetitive behaviors, such as excessive hand washing or constant counting of objects. While we know that OCD tends to run in families, it’s been frustratingly difficult to identify specific genes that influence OCD risk.

Now, an international research team, partly funded by NIH, has made progress thanks to an innovative genomic approach involving dogs, mice, and people. The strategy allowed them to uncover four genes involved in OCD that turn out to play a role in synapses, where nerve impulses are transmitted between neurons in the brain. While more research is needed to confirm the findings and better understand the molecular mechanisms of OCD, these findings offer important new leads that could point the way to more effective treatments.

While earning her Ph.D. in clinical psychology, Dylan Gee often encountered children and adolescents battling phobias, panic attacks, and other anxiety disorders. Most overcame them with the help of psychotherapy. But not all of the kids did, and Gee spent many an hour brainstorming about how to help her tougher cases, often to find that nothing worked.

What Gee noticed was that so many of the interventions she pondered were based on studies in adults. Little was actually known about the dramatic changes that a child’s developing brain undergoes and their implications for coping under stress. Gee, an assistant professor at Yale University, New Haven, CT, decided to dedicate her research career to bridging the gap between basic neuroscience and clinical interventions to treat children and adolescents with persistent anxiety and stress-related disorders.

For people struggling with severe depression, antidepressants have the potential to provide much-needed relief, but they often take weeks to work. That’s why there is growing excitement about reports that the anesthetic drug ketamine, when delivered intravenously in very low doses, can lift depression and suicidal thoughts within a matter of hours. Still, there has been reluctance to consider ketamine for widespread treatment of depression because, even at low doses, it can produce very distressing side effects, such as dissociation—a sense of disconnection from one’s own thoughts, feelings, and sense of identity. Now, new findings suggest there may be a way to tap into ketamine’s depression-fighting benefits without the side effects.

In a mouse study published in the journal Nature, an NIH-funded research team found that the antidepressant effects of ketamine are produced not by the drug itself, but by one of its metabolites—a substance formed as the body breaks ketamine down. What’s more, the work demonstrates that this beneficial metabolite does not cause the risky dissociation effects associated with ketamine. While further development and subsequent clinical trials are needed, the findings are a promising step toward the development of a new generation of rapid-acting antidepressant drugs.

Each year, about 100,000 American adolescents and young adults, their lives and dreams ahead of them, experience their first episode of psychosis, a symptom of schizophrenia and other mental illnesses characterized by dramatic changes in perception, personality, and ability to function [1]. This often-terrifying experience, which can last for months, will prompt some to seek help from mental health professionals, whose services can in many situations help them get back on track and reduce the risk of relapse. Still, for far too many young people and their families, the search for help is riddled with long delays, contradictory information, and inadequate treatment in a mental health system whose resources have been stretched thin.

There’s got to be a better way to reach more of these young people, and, now, results of a major NIH-supported clinical study point to a possible way to get there [2]. In this large study, published in the American Journal of Psychiatry, teams of mental health specialists partnered with young people and their families to create individualized treatment plans. After two years of follow-up, researchers found that this personalized, team-based approach to care had helped more young people stick with treatment, feel better about their quality of life, return to school and work, and seek follow-up help than standard care involving a single clinician.

Many studies show the longer that people with psychotic episodes go untreated, the harder it is to stabilize their symptoms and the more problems they develop. A common presentation is schizophrenia, a persistent, severe brain disorder that often can be diagnosed only months or even years after a first psychotic episode. Schizophrenia affects 1.1 percent of Americans ages 18 and older, and currently accounts for about 30 percent of all spending on mental health treatment [3].

As many as one in five U.S. teenagers experience an episode of major depression by the time they turn 18. Sadly, depression among teens often goes unrecognized, increasing the risk of suicide, substance abuse, and many other problems. Even among those who are diagnosed, few receive proper treatment. But now there’s a ray of hope from a new NIH-funded study that’s found success using a team approach that pairs depressed teens and their parents with a counselor [1].

Faced with a shortage of psychiatrists who specialize in child mental health, a multidisciplinary team from the Seattle Children’s Research Institute, University of Washington School of Medicine, and Group Health in Seattle decided to use a strategy called “collaborative care” to treat depressed teenagers. There are more than 70 clinical trials showing that team-based care approaches work well for adults with depression, but there were only two such previous studies in teens—and results were mixed.

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About the NIH Director

Francis S. Collins, M.D., Ph.D., was appointed the 16th Director of NIH by President Barack Obama and confirmed by the Senate. He was sworn in on August 17, 2009. On June 6, 2017, President Donald Trump announced his selection of Dr. Collins to continue to serve as the NIH Director.